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Morphine excitation in the cerebral cortex.

B Bioulac, J P Lund, E Puil

Canadian Journal of Physiology and Pharmacology

|August 1, 1975

Summary

Morphine weakly excites cerebral cortex neurons in cats, an effect blocked by methylatropine but not naloxone. This suggests a muscarinic mechanism for morphine-induced excitation, distinct from its analgesic properties.

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Area of Science:

Neuroscience
Pharmacology
Neurochemistry

Background:

Morphine, a potent opioid analgesic, has complex effects on the central nervous system.
Previous research suggests potential interactions between opioids and cholinergic systems in the brain.

Purpose of the Study:

To investigate the effects of microiontophoretic morphine administration on cholino-excitable neurons in the feline cerebral cortex.
To elucidate the potential muscarinic receptor involvement in morphine's cortical actions.

Main Methods:

Microiontophoresis of morphine, acetylcholine, methylatropine, and glutamate onto single cortical neurons in decerebrate cats.
Recording neuronal firing rates in response to iontophoretic applications.
Assessing the effects of antagonists on evoked neuronal responses.

Main Results:

Morphine induced a weak excitation of cholino-excitable cortical neurons, which increased with repeated doses.
This excitation was not antagonized by naloxone, an opioid antagonist.
Methylatropine, a muscarinic antagonist, blocked morphine-induced excitation but not glutamate-evoked excitation.
Morphine depressed glutamate-evoked firing in neurons not responsive to acetylcholine.

Conclusions:

The findings suggest a muscarinic component to morphine's action in the cerebral cortex.
This muscarinic effect may contribute to morphine-induced excitation and convulsions, but not analgesia.
Opioid-induced central nervous system excitation may involve interactions with cholinergic pathways.

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